An AT1-receptor antagonist and an angiotensin-converting enzyme inhibitor protect against hypoxia-induced apoptosis in human aortic endothelial cells through upregulation of endothelial cell nitric oxide synthase activity.

The protective effects and roles of AT1-receptor antagonists (AT1-RA) or angiotensin-converting enzyme inhibitors (ACEI) on vascular endothelial cell (EC) injury during hypoxia are not entirely known. Therefore, we investigated these effects and mechanisms in human aortic (HA) EC. DNA fragmentation, Lactate dehydrogenase (LDH) release, and caspase-3 activity were measured in cultured HAEC after exposure to hypoxia in the presence or absence of an AT1-RA (candesartan, CS) and/or an ACEI (temocaprilat, TC).

Alpha-tocopherol prevents apoptosis of vascular endothelial cells via a mechanism exceeding that of mere antioxidation.

Alpha-tocopherol has been reported to exert an anti-atherogenesis effect. We attempted to clarify the effect of alpha-tocopherol-both as an antioxidant and as a nonantioxidant--on apoptosis induced by oxidized low-density lipoprotein (LDL) or oxysterols. Oxidized LDL and oxysterols induced necrosis and/or apoptosis of vascular endothelial cells.

A comparison of shaping ability using ProFile, GT file, and Flex-R endodontic instruments in simulated canals.

A total of 160 resin-simulated canal blocks with 20-degree or 30-degree curvature were prepared by ProFile rotary instruments, GT rotary files, and the balanced force technique with Flex-R files. Using an image analysis computer application, the pre- and postoperative images were stored and superimposed, and then the amount of material removed from the preoperative inner and outer curved walls was measured at five levels in the apical 5 mm of the canal. The time required for canal preparation, including irrigation, and the time taken to change instruments was recorded.